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Project description:Photobiomodulation (PBM) with blue light induces a biphasic dose response curve in proliferation of immortalized human keratinocytes (HaCaT), with a maximum proliferative effect reached with 7.5min (10.35J/cm2). The aim of this study was to test the photobiomodulatory effect of 10.35J/cm2 blue light irradiation on cell proliferation, ROS production and gene expression at different time points after irradiation of HaCaT cells in vitro and to compare the results with the anti-proliferative phase of PBM using blue light with 41.4J/cm2. For 10.35J/cm2 cell proliferation was increased for all measured harvesting time points up to at least 24h after irradiation. ROS concentration was increased 30min after irradiation. However, already 1h after irradiation, cells were able to decrease ROS and stabilize the concentration to the basal level. The sudden increase in ROS was even higher when compared to 41.4J/cm2. However, gene expression analysis did not indicate any sign of apoptosis and even indicated an activation of cell survival mechanisms. Furthermore, comparable to 41.4J/cm2, aryl hydrocarbon receptor (AHR) “battery genes” showed a deregulation after blue light irradiation strengthening the hypothesis of AHR as possible target for blue light irradiation.
2019-10-01 | GSE89084 | GEO
Project description:Photobiomodulation (PBM) with blue light induces a biphasic dose response curve in proliferation of immortalized human keratinocytes (HaCaT), with a maximum proliferative effect reached with 7.5min (10.35J/cm2). The aim of this study was to test the photobiomodulatory effect of 10.35J/cm2 blue light irradiation on cell proliferation, ROS production and gene expression at different time points after irradiation of HaCaT cells in vitro and to compare the results with the anti-proliferative phase of PBM using blue light with 41.4J/cm2. For 10.35J/cm2 cell proliferation was increased for all measured harvesting time points up to at least 24h after irradiation. ROS concentration was increased 30min after irradiation. However, already 1h after irradiation, cells were able to decrease ROS and stabilize the concentration to the basal level. The sudden increase in ROS was even higher when compared to 41.4J/cm2. However, gene expression analysis did not indicate any sign of apoptosis and even indicated an activation of cell survival mechanisms. Furthermore, comparable to 41.4J/cm2, aryl hydrocarbon receptor (AHR) “battery genes” showed a deregulation after blue light irradiation strengthening the hypothesis of AHR as possible target for blue light irradiation.
2019-10-01 | GSE89083 | GEO
Project description:Photobiomodulation (PBM) with blue light induces a biphasic dose response curve in proliferation of immortalized human keratinocytes (HaCaT), with a maximum proliferative effect reached with 7.5min (10.35J/cm2). The aim of this study was to test the photobiomodulatory effect of 10.35J/cm2 blue light irradiation on cell proliferation, ROS production and gene expression at different time points after irradiation of HaCaT cells in vitro and to compare the results with the anti-proliferative phase of PBM using blue light with 41.4J/cm2. For 10.35J/cm2 cell proliferation was increased for all measured harvesting time points up to at least 24h after irradiation. ROS concentration was increased 30min after irradiation. However, already 1h after irradiation, cells were able to decrease ROS and stabilize the concentration to the basal level. The sudden increase in ROS was even higher when compared to 41.4J/cm2. However, gene expression analysis did not indicate any sign of apoptosis and even indicated an activation of cell survival mechanisms. Furthermore, comparable to 41.4J/cm2, aryl hydrocarbon receptor (AHR) “battery genes” showed a deregulation after blue light irradiation strengthening the hypothesis of AHR as possible target for blue light irradiation.
2019-10-01 | GSE89085 | GEO
Project description:Photobiomodulation by blue light induces a dose dependent biphasic proliferation curve in human keratinocytes
| PRJNA350268 | ENA
Project description:Potent neuroprotective effects of photobiomodulation with 670 nm red light (RL) have been demonstrated in several models of retinal disease. RL improves mitochondrial metabolism, reduces retinal inflammation and oxidative cell stress, showing its ability to enhance visual function. However, the current knowledge is limited to the main hypothesis that the respiratory chain complex IV, cytochrome c oxidase, serves as the primary target of RL. Here, we demonstrate a comprehensive cellular, molecular, and functional characterization of neuroprotective effects of 670 nm RL and 810 nm near-infrared light (NIRL) on blue light damaged murine primary photoreceptors. We show that respiratory chain complexes I and II are additional PBM targets, besides complex IV, leading to enhanced mitochondrial energy metabolism. Accordingly, our study identified mitochondria related RL- and NIRL-triggered defense mechanisms promoting photoreceptor neuroprotection. The observed improvement of mitochondrial and extramitochondrial respiration in both inner and outer segments is linked with reduced oxidative stress including its cellular consequences and reduced mitochondria-induced apoptosis. Analysis of regulatory mechanisms using gene expression analysis identified upregulation ?-crystallins that indicate enhanced production of proteins with protective functions that point to the rescued mitochondrial function. The results support the hypothesis that energy metabolism is a major target for retinal light therapy.
| S-EPMC7177783 | biostudies-literature
Project description:BackgroundPhotobiomodulation consists of inducing healing by irradiating light. This scoping review investigates the effect of blue light on the healing process.MethodsThe MEDLINE, Web of Science, Scopus, and CINAHL databases were searched. Two reviewers independently examined the search results and extracted data from the included studies. A descriptive analysis was performed.ResultsTwenty-two articles were included. Studies were categorized as in vitro/mixed, preclinical, and clinical. The power density used was 10-680 mW/cm2 in most of the in vitro/preclinical studies, the irradiation time ranged from 5 s to 10 min, and different wavelengths and energy densities were used. In clinical studies, the wavelength ranged from 405 to 470 nm, and the energy density varied from 1.5 to 30 J/cm2.ConclusionsA low energy density (<20 J/cm2) was able to stimulate the different cell types and proteins involved in healing, while a high energy density, 20.6-50 J/cm2, significantly reduced cell proliferation, migration, and metabolism. There is a great variety of device parameters among studies, and this makes it difficult to conclude what the best technical specifications are. Thus, further studies should be performed in order to define the appropriate parameters of light to be used.
| S-EPMC9959862 | biostudies-literature
Project description:Curcumin is a widely known natural phytochemical from plant Curcuma longa. In recent years, curcumin has received increasing attention because of its capability to induce apoptosis and inhibit cell proliferation as well as its anti-inflammatory properties in different cancer cells. However, the therapeutic benefits of curcumin are severely hampered due to its particularly low absorption via trans-dermal or oral bioavailability. Phototherapy with visible light is gaining more and more support in dermatological therapy. Red light is part of the visible light spectrum, which is able to deeply penetrate the skin to about 6 mm, and directly affect the fibroblast of the skin dermis. Blue light is UV-free irradiation which is fit for treating chronic inflammation diseases. In this study, we show that curcumin at low concentrations (1.25-3.12 μM) has a strong anti-proliferative effect on TNF-α-induced psoriasis-like inflammation when applied in combination with light-emitting-diode devices. The treatment was especially effective when LED blue light at 405 nm was combined with red light at 630 or 660 nm, which markedly amplified the anti-proliferative and apoptosis-inducing effects of curcumin. The experimental results demonstrated that this treatment reduced the viability of human skin keratinocytes, decreased cell proliferation, induced apoptosis, inhibited NF-κB activity and activated caspase-8 and caspase-9 while preserving the cell membrane integrity. Moreover, the combined treatment also down-regulated the phosphorylation level of Akt and ERK. Taken together, our results indicated that the combination of curcumin with LED blue light united red light irradiation can attain a higher efficiency of regulating proliferation and apoptosis in skin keratinocytes.
| S-EPMC4575166 | biostudies-literature
Project description:Blue light regulates biological function in various cells, such as proliferation, oxidative stress, and cell death. We employed blue light illumination on human umbilical vein endothelial cells utilizing a LED device at 453 nm wavelength and revealed a novel biphasic response on human umbilical vein endothelial cells (HUVECs). The results showed that low fluence blue light irradiation promoted the fundamental cell activities, including cell viability, migration and angiogenesis by activating the angiogenic pathways such as the VEGF signaling pathway. In contrast, high fluence illumination caused the opposite effect on those activities by upregulating pro-apoptotic signaling cascades like ferroptosis, necroptosis and the p53 signaling pathways. Our results provide an underlying insight into photobiomodulation by blue light and may help to implement potential treatment strategies for treating angiogenesis-dependent diseases.
| S-EPMC8301484 | biostudies-literature
Project description:The COX-2/PGE2 axis can play roles in mediating the progression of tumor. COX-2 induction was observed in oral cancer. In our previous study, we found Staphylococcus aureus, a pathogen prevalent in oral cancer, can activate the COX-2/PGE2 pathway in human oral keratinocyte (HOK) cells. Here, we investigated the proliferation of HOK cells affected by COX-2 induction and the role of COX-2 induction in the malignant transformation of HOK cells. We found S. aureus was able to facilitate HOK cell proliferation through upregulating COX-2 expression. With the induction of COX-2, expression of oral cancer-associated genes cyclin D1 was upregulated and p16 was downregulated. Transcriptome analysis showed that the "NF-kappa B signaling pathway" and "TNF signaling pathway" had the highest enrichment of differentially expressed genes (DEGs) with COX-2 over-expression. Seven upregulated genes (jun, tlr4, cxcl1, lif, cxcl3, tnfrsf1β, and il1β) in these two pathways were critical for the increased proliferation of HOK cells and might be associated with COX-2. Malignant transformation of cells was evaluated by soft agar colony formation assay and S. aureus infection promoted HOK cell colony formation. These results suggest the potential of S. aureus to induce the infection-associated malignant transformation of oral epitheliums through COX-2 activation.
| S-EPMC6691923 | biostudies-literature
Project description:The cell viability and apoptosis of tumor U937 cells treated by blue light (BL) irradiation have been examined. BL irradiation can specially inhibit the proliferation and promote the apoptosis of U937 cells, relating to the production of reactive oxygen species (ROS) and the decline of mitochondrial membrane potential (ΔΨm). The apoptosis is further associated with varying downregulated B-cell lymphoma-extra large (Bcl-XL) and B-cell lymphoma 2 (Bcl-2) genes, upregulated Bcl-2-associated X (Bax) gene, the activation of caspase-3 and caspase-9, and the cleavage of poly (ADP-ribose) polymerase (PARP) by the BL irradiation process. Moreover, BL irradiation induced proliferation inhibition is higher than that treated by a common chemotherapeutic drug of homoharringtonine (HHT). When we synergize BL irradiation with HHT (BL-HHT), a higher proliferation inhibition is obtained than that treated by BL irradiation or HHT alone. These results are helpful for establishing a low toxicity and high efficiency strategy of BL irradiation for clinical treatment of acute myeloid leukemia, not limited to U937 cells.
| S-EPMC5983758 | biostudies-literature